News tips from the Journal of Neuroscience

The synaptic vesicle protein synaptobrevin is an essential component of the vesicle release machinery along with its plasma membrane partners (syntaxin and SNAP-25), although in the absence of synaptobrevin release it is not completely eliminated. DeŠk et al. explored the structural requirements of synaptobrevin function by using engineered constructs to rescue release in hippocampal neurons cultured from synaptobrevin-deficient mice. Cellubrevin, which has divergent N- and C-terminal domains, but a nearly identical central SNARE motif with synaptobrevin, rescued transmission. An electrostatic interaction between arginine (R) and glutamine (Q) in the "zero layer" of each SNARE was not essential because an R-Q substitution in synaptobrevin rescued evoked and spontaneous release. However, spacing between the SNARE motif and C-terminal transmembrane domain was critical. Synaptobrevin with a 12-residue insertion between the SNARE motif and the transmembrane region provided only partial rescue, and synaptobrevin with a 24-residue insertion failed to rescue any function.

Neonatal rats learn rapidly to use odors to identify their mother. Pups are aided in this task by a boost in odor-preference learning and a deficit in odor-aversion learning, in a sensitive period before postnatal day 10 (P10). In this week's Journal, Moriceau et al. investigated the role of corticosterone (CORT) during the sensitive period. Rat pups that received a shock paired with odor at P8 learned an odor preference. However, systemic CORT injection 24 h and 30 min before pairing prematurely ended the sensitive period, resulting in odor aversion learning and activation of the amygdala. Conversely, removal of CORT by adrenalectomy prolonged the sensitive period. After adrenalectomy, P12 rats learned odor-shock preference rather than aversion and displayed increased olfactory bulb activity. The authors postulate that CORT acts as an amygdalar switch that favors the emergence of olfactory fear conditioning.

Mammalian ovulation is the culmination of a complex neurohormonal signaling pathway. Gonadotropin-releasing hormone (GnRH) is normally under tonic negative feedback control, but estrogen triggers a GnRH/luteinizing hormone (LH) surge that leads to ovulation. This week, Smith et al. investigated the kisspeptins as potential mediators of this signaling cascade. This family of neuropeptides, encoded by the Kiss1 gene, is expressed in neurons of the anteroventral periventricular nucleus (AVPV) and the arcuate nucleus. The authors hypothesized that activation of Kiss1 neurons is linked to the GnRH/LH surge. In rats, estradiol acted at the two nuclei with opposite effects. Kiss1 mRNA expression was inhibited in the arcuate nucleus but upregulated in the AVPV. The latter coincided with expression of the immediate early gene Fos, consistent with their activation during the GnRH/LH surge. As necessary for their hypothesis, Kiss1 neurons also expressed the estradiol receptor ERa.

In this week's Journal, Assanah et al. tested the potential of glial progenitor cells as cells of origin for malignant glial tumors. The authors injected adult rat brain white matter with a retrovirus driving expression of green fluorescent protein (GFP), and platelet-derived growth factor B (PDGF-B), a mitogen expressed by glial progenitors and in human gliomas. All injected animals developed brain tumors that resembled malignant glioblastomas. Interestingly, the tumors contained not only infected cells but also uninfected cells, suggesting a role for autocrine and paracrine messengers in tumor growth. Progenitors infected with a retrovirus expressing GFP alone did not cause tumors, rather these cells differentiated into oligodendrocytes. When two viruses expressing PDGF or GFP alone were coinjected, however, GFP-labeled progenitor cells in the tumor environment were recruited to proliferate and migrate, contributing to the tumor in what would appear to be a deadly game of follow the leader.

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Last reviewed:
By John M. Grohol, Psy.D. on
21 Feb 2009
Published on PsychCentral.com. All rights reserved.